Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Microbial Pathogens > Bacterial Pathogens (1-3) > Flashcards

Bacterial Pathogens (1-3) Flashcards

1
Q

What is a pathogen?

A

A microbe roar is able to cause disease in a plant, animal or insect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is pathogenicity?

A

The ability to produce disease in a host organism
→ expressed through their virulence
→ determinants of virulence: genetic, biochemical or structural features that enable it to produce a disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the underlying mechanisms of bacterial pathogenicity?

A

Ability to invade → colonisation (adherence and multiplication), ability to overcome host defence, extracellular substances that facilitate entry
→ e.g. adhesins like fimbiae

Ability to produce toxins → exotoxins: released from bacteria e.g. Cholera toxin
→ endotoxins: cell-associated e.g. LPS, capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can pathogens enter the human body?

A

Respiratory → inhalation
Gastro-intestinal → ingest
Urinary/genital tracts

via insect bites or accidental/surgical trauma to skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some examples of human primary pathogen transmission?

A

Bordetella pertussis → whooping cough, requires contact with infectious material

Neisseria gonorrhoeae → sexually transmitted, requires direct person-to-person mucosal contact - man only natural host so dies in environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the environment that a pathogen can colonise effect?

A

The environments that can be colonised by a pathogen are critical in determining its reservoirs and potential modes of transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a psychrophile, psycotroph, mesophile and thermophile?

A

Psychrophile → microbes that grow best at low temps (optimum 10-15C)
Psychotroph → able to grow at low temps, but prefer moderate (optimum 15-30C)
Mesophile → most bacteria (optimum 30-40C)
Thermophile → optimum 45-70C

(phile = loves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are bacterial growth curves symmetrical?

A

No → steady increase to optimum then crash after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the acclimation phase in cold shock?

A

A downshift in temp causes inhibition of most protein synthesis - has to produce new machinery (ribosomes)
→ causes a growth lag - acclimation phase
→ a group of cold shock proteins (Csp) are dramatically induced - essential for cell growth to resume at the low temp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are E. coli cold shock proteins?

A

Involved in ensuring ribosome function and DNA/RNA synthesis

Class I → >10-fold induction
→ e.g. CspA family: CspA RNA chaperones, CspB/CspC RNA&DNA chaperone, RNP ribonuclease
Class II → <10-fold induction
→ e.g. RecA: recombination factor, H-NS: nucleoid-assocaited DNA-binding protein

→ conditioning ribosome for cold temps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Listeria?

A

Non-spore forming Gram +ve bacilli
→ causes listeriosis
→ serious for pregnant women and immunocompromised people
→ widespread in environment, vegetation, water4, soil, wild/domestic animals, fish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is unique about Listeria bacterial growth?

A

Capable of growth over a wide range of temperatures (4-40C)
→ e.g. can survive in fridge

→ can be spread through contaminated food: meats, unpasteurised milk, vegetables (coleslaw) - foods that require no further heat treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What virulence factors of Listeria is involved in the invasion of mammalian cells?

A

Internalin A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What virulence factors of Listeria are required for its escape from membrane vacuole?

A

LLO (listeriolysin) → pore-forming cytotoxin punches holes in membrane - surrounded by vacuole upon entry so must degrade

PI-PLC (PlcA) → an enzyme that removes charged head groups from phospholipids

double membrane vacuole:
PC-PLC (PlcB) → a phospholipase that cleaves the head group from many kinds of lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What virulence factors of Listeria are required for movement through the cytoplasm (cell-cell spread)?

A

ActA → stimulates host cell actin polymerisation (in wrong place ie. surface of bacterium), actin tail forms and propels bacterium through cytoplasm
→ causes projections from the host cell enter adjacent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are Listeria virulence factors regulated?

A

PrfA → positive regulator of virulence genes
→ may repose to temp
→ DNA binding protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is Listeria controlled in food?

A

Can grow and multiply at normal refrigeration temps, freezing, and relatively high cooking temps - also can grow in other food preservatives

→ controlled by: heating at 70C for 2 mins, avoiding unpasteurised milk, avoid coleslaw and deli meats, cook meat thoroughly and reheat after refrigeration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Legionella pneumophila?

A

Motile, aerobic Gram -ve rod
→ cause Legionnaire’s disease - a form of bacterial pneumonia
→ normal environment: biofilm (in air con) or inside protozoa - humans accidental host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does pH affect growth rate?

A

Growth rate curve symmetrical around the optimum pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the terms used in relation to pH and growth?

A

Acidophiles → grow at an optimum below neutrality (>7pH)
Neutrophiles → grow best at neutral pH
Alkaliphiles → grow best under alkali conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is an obligate acidophile?

A

Require a low pH for growth
→ their membranes dissolve and cells lyse at neutrality
→ several genera of archaea

22
Q

What are obligate alkaliphiles?

A

Can grow around pH 10
→ Na+ gradient (instead of pmf = proton motive force = pH gradient and electrochemical gradient) supplies the energy

23
Q

What does the intracellular pH for most organisms need to be?

A

Intracellular pH mostly needs to stay around neutrality
→ to prevent destruction of acid or alkali labile macromolecules

anomalies: extreme acidophiles and alkaliphiles
→ their internal pH can very by several units from neutrality

24
Q

What are the problems posed by acidic conditions?

A

3 major aspects of cell function cane affected by acidic conditions
1. the capacity for nutrient acquisition and energy generation
2. cytoplasmic pH homeostasis
3. protection of proteins and DNA → critical for cell survival

25
How can proteins and DNA be protected in acidic conditions?
Chaperone proteins and alkalisation of the periplasm (periplasm in Gram -ve cell walls, between outer and cytoplasmic membrane)
26
What is *Helicobacter pylori*?
Gram -ve curved rod, highly motile 4-7 polar flagella Cause gastric and duodenal ulcers (associated with development of gastric cancer) Reservoir: lining of the stomach Main virulence factors: flagella, urease, adhesions,
27
How do we know *Helicobacter pylori* causes ulcers?
Known to be associated but there was no animal model so couldn't follow usual method to confirm Koch's postulates → Barry Marshall drank culture of H. pylori - 2 weeks later had inflamed stomach
28
How does *H. pylori* survive in the acidic pH of the stomach?
Organism doesn't colonies the lumen but the mucin layer that covers the stomach → mucus resists diffusion of protons from stomach acid due to -ve sulphated polysaccharides However must reach the mucin layer so needs: → motility → short term pH protection using enzyme urease
29
What does the enzyme urease do?
Urease takes up urea (waste product) and hydrolyses it producing ammonia and CO2 → ammonia neutralises stomach acid in its immediate vicinity → urease is intraceullular so exports ammonia to periplasm where pH can rise ~ pH 6
30
How does *Helicobacter pylori* give rise to ulcers?
Uses urease to protect it from stomach acid during transit → colonises mucin layer Products provoke inflammatory response that ultimately damage the mucosa BabA: adhesin that recognises Lewis b antigen which binds sulphated mucin sugars on epithelial cells NAP: neutrophil activation protein - activates neutrophils, leads to inflammation VacA: vacuolating cytotoxin - produces large vacuoles in mammalian cells
31
What is *Salmonella typhimurium*?
Characteristics: Gram-negative rod, motile Disease: gastroenteritis, diarrhoea Reservoir: human carriers, livestock animals, reptiles Transmission: contaminated food Main virulence factors: acid tolerance response, adhesins, invasion of mucosal cells, type III secretion system Prevention: proper food handling Treatment: antibiotics
32
What is the *Salmonella typhimurium* acid tolerance response?
Allows S. typhimurium to survive in the acid environment of the stomach Rapid exposure to low pH → rapid die-off More gradual exposure to low pH (i.e. adapted to pH6 first) → cells can survive down to pH 3
33
What cells regulate acid shock proteins?
Fur = the regulator of iron acquisition genes → Fur senses pH and iron separately → iron is an essential micro-nutrient
34
How can pH tolerance in Gram + bacteria affect human health?
mutans Streptococci → causes dental caries - organisms produce acid and can survive at low pH Listeria → causes listeriosis - drop in pH activates haemolysin permitting its escape from the phagosome, capable of surviving acid stress in food like cottage cheese, yoghurts and orange juice Rhodococcus equi → causes broncopneumonia in horses - encounters low pH in alveolar macrophages - acid resistant
35
What are the mechanisms of acid resistance in Gram positive bacteria?
Proton pumps → F1F2-ATP ases, GAD Protein/DNA repair → some chaperones Regulators → e.g. several 2 component systems (sensor + response) in Listeria Altered metabolism → e.g. a quorum sensing system & biofilm - acid tolerance in S. mutans Envelope alterations → e.g. S. mutans increased levels of mono-saturated and longer chain fatty acids at pH5 than pH7 Production of alkali → e.g. urease production (increased pH)
36
What are obligate aerobes and anaerobes?
Aerobes: require O2 for growth → they use O2 as a final electron acceptor in aerobic respiration Anaerobes: don't need O2 as a nutrients (O2 is toxic - kills or inhibits growth) → may live by fermentation, aerobic respiration, bacterial photosynthesis or methanogensis
37
What are facultative anaerobes?
Organisms that can switch between aerobic and anaerobic metabolism → no O2 - fermentation, anaerobic respiration → O2 - aerobic respiration
38
What are aerotolerant anaerobes?
Bacteria with an exclusively anaerobic (fermentative) type of metabolism but are insensitive to presence of O2 → live by fermentation alone whether of not O2 is present
39
How do flavoproteins react with O2?
Oxidation of flavoproteins results in the formation of H2O2 (peroxide) and small quantities of O2- superoxide (an even more toxic free radical) → ROS can damage cells - will kill the cell if nothing is done about them
40
How is the potential for lethal accumulation of superoxide prevented in aerobes?
The enzyme superoxide dismutase → all organisms which can live in the presence of O2 contain superoxide dismutase
41
How is peroxide decomposed?
By the enzyme catalase → certain aerotolerant bacteria lack catalase so they use peroxidase enzymes (derive e- from NADH2 producing water)
42
Why do obligate anaerobes undergo lethal oxidations by various oxygen radicals when exposed to O2?
They lack superoxide dismutase and catalase → can't protect against ROS
43
What is the action of superoxide dismutase, catalase and peroxidase?
Detoxify oxygen radicals Superoxide dismutase: [O₂-] + [O₂-] (+2H+) → O₂ + H₂O₂ Peroxidase: H₂O₂ + O₂ (+ NADH + H+ → NAD+) → 2H₂O Catalase: 2H₂O₂ → 2H₂O + O₂
44
How does *Clostridium spp.* obtain ATP?
Substrate-level phosphorylation → most lack respiratory chain cytochromes, catalase, peroxidase and superoxide dismutase
45
What is *Clostridium botulinum*?
Commonly found in soil samples and aquatic sediments → causative agent of botulinum food poisoning → releases exotoxin bolutlinum - extremely potent + can form spores → poorly canned foods create anaerobic environment - unskilled spores germinate and produce toxin
46
What is botulism?
Result of ingesting bacterially produced neurotoxins → the toxins block the release of neurotransmitter acetylcholine → resulting in double vision, slurred speech, decreased saliva, general weakness → paralysis with accompanying respiratory failure can be fatal
47
What are the types of exotoxin produced by *Clostridium botulinum*?
7 - A, B, C1, D, E, F, G → A, B, E, and F are the most toxic to humans (often released in inactive form, proteolytic cleavage activates them) → A is the most potent exotoxin known
48
What is the mode of action of botulinum toxin?
Botulinum toxin has heavy chain (HC) and light chain (LC) → HC binds toxin to the presynaptic receptor - toxin enters the cell → disulphide bond cleaved - liberates the LC into cytoplasm and endosomal compartment → cleaves the SNARE proteins (involved in vesicle docking) → prevents fusion of acetylcholine vesicles at the cell membrane Prevents the release of Act → no stimulus → can't contract → flaccid paralysis
49
What is *Clostridium tetani*?
Causative agent of tetanus (lockjaw) → result of trauma/puncture wound leading to tissue contamination → caused by release of single antigenic type endotoxin by C. tetani - circulates in blood and adheres to neuronal receptors → fixes to gangliosides - blocking release of the neurotransmitters glycine and y-amino butyric acid (GABA) → muscles permanently contracted
50
How does the tetanus toxin work?
Tetanus toxin made up of a heavy chain (HC) required for cell entry and a light chain (LC) which causes disease → C-terminal domain of the HC binds to gangliosides, N-terminal domain allows LC to cross into cell cytoplasm → LC interrupts the release of neurotransmitters → cleaves SNARE proteins - GABA and glycine containing vesicles can't dock thus no neurotransmitter released Glycine usually induces muscle relaxation - constant release of Act - muscles permanently contracted
51
How are hosts affected by *Clostridium tetani*?
Toxin causes tetanus → host usually dies from respiratory paralysis heroin addicts are particularly susceptible
52
What is *Clostridium difficile*?
Gram positive, obligately anaerobic, spore forming Antibiotic use reduces normal microbiota → *C. diff* overgrows produces toxins A and B → A and B - large exotoxins that modify host cell membrane G proteins Toxins cause: diarrhoea and lesions on colon surface → coalesce forming tissue damage - pseudomembranous colitis → can be rapidly fatal

Microbial Pathogens (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions